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JCI online early table of contents: Sept. 13, 2010
Date:9/13/2010

To analyze more fully the role of PPAR-alpha and gamma in lipotoxic cardiomyopathy, Ira Goldberg and a team of scientists at Columbia University, New York, investigated heart function in mice in which PPAR-gamma was over-expressed in the heart (a model of cardiomyopthy) and PPAR-alpha had been genetically deleted. They found that deletion of PPAR-alpha improved heart function in this model, but surprisingly, this improvement was associated with increased levels of FAO and increased expression of genes involved in lipid storage. The improvement in heart function was related to a differential distribution of lipid into larger droplets, as well as reduced levels of cellular stress in the heart muscle. The researchers believe that these data demonstrate that increased lipid storage and FAO levels are not inherently toxic to the heart, and that targeting of these processes may represent a promising therapeutic strategy for lipotoxic cardiomyopathy.

TITLE:

PPARγ-induced cardiolipotoxicity in mice is ameliorated by PPARα deficiency despite increases in fatty acid oxidation

AUTHOR CONTACT:
Ira J. Goldberg,
Columbia University, New York, New York, USA.
Phone: 212.305.5961; Fax: 212.305.3213; E-mail: ijg3@columbia.edu.
View this article at: http://www.jci.org/articles/view/40905?key=78f0274db36a17a0c8f1


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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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